In mammals, injury triggers an organised complex cascade of cellular and biochemical events that result in a healed wound. Wound healing is a complex dynamic process that results in the restoration of anatomic continuity and function; an ideally healed wound is one that has returned to normal anatomic structure, function and appearance.
Infection of wounds by bacteria delays the healing process, since bacteria compete for nutrients and oxygen with macrophages and fibroblasts, whose activity are essential for the healing of the wound. Infection results when bacteria achieve dominance over the systemic and local factors of host resistance. Infection is therefore a manifestation of a disturbed host/bacteria equilibrium in favour of the invading bacteria. This elicits a systemic septic response, and also inhibits the multiple processes involved in wound healing. Lastly, infection can result in a prolonged inflammatory phase and thus slow healing, or may cause further necrosis of the wound. The granulation phase of the healing process will begin only after the infection has subsided.
The persistent presence of bacteria in injured tissue results in the prolonged elevation of proinflammatory cytokines such as interleukin-1 and tumour necrosis factor alpha (TNF-α). This in turn causes increases in the levels of matrix metalloproteinases, a decreased level of tissue inhibitors to the metalloproteinases (TIMP), and a decreased production of growth factors.
Chronically contaminated wounds all contain a tissue bacterial flora These bacteria may be indigenous to the patient or might be exogenous to the wound. Closure, or eventual healing of the wound is often based on a physician's ability to control the level of this bacterial flora.
Current methods used to identify bacterial infection rely mainly on judgement of the odour and appearance of a wound. With experience, it is possible to identify an infection in a wound by certain chemical signs such as redness or pain. Some clinicians take swabs that are then cultured in the laboratory to identify specific organisms, but this technique takes time. The prior art also describes the use of certain proteases as an indicator of healing status.
If clinicians could respond to wound infection as early as possible the infection could be treated topically as opposed to having to use antibiotics. This would also lead to less clinical intervention/hospitalisation and would reduce the use of antibiotics and other complications of infection.
There is thus a long felt need for a prognostic aid that would assist in predicting clinical infection of a wound prior to obvious clinical symptoms of infection. Such a prognostic aid would allow early intervention with suitable treatment (e.g. a topical antimicrobial treatment) before wound chronicity sets in. There is also a need for a diagnostic aid that would assist in the early diagnosis of clinical infection, preferably allowing diagnosis prior to obvious clinical symptoms of infection.